The object of this research is to determine if angiotensin's central nervous effects are dependent on sodium and how the hormone affects sodium metabolism. Main findings to date include: 1. Central angiotensin injections evoke water intake, ADH release and a fall in plasma renin activity in rats kept on normal high and low Na ion intakes; this response is favorable when dietary Na ion is high, but not when low. 2. Angiotensin drinking after CSF injections does not require far lateral hypothalamic sites needed for osmotic drinking. 3. Combined blockade of peripheral and central angiotensin receptors does not impede water intake after water deprivation. 4. Central injections of angiotensin antiserum do not affect food and water intake or urine volume and electrolytes over a 24 hr period in normally hydrated or cellular dehydrated rats. 2. The same parameters are unaffected by central injections of vasopressin or vasopressin antiserum. 6. Choroid plexi from normal, water deprived or hypovolemic rats have similar renin activities when measured in an in vitro assay standardized for (Na ion), osmolality and protein. Current work includes: 1. CSF sampling from conscious, unrestrained rats receiving i.v. infusion of iso- or hypertonic NaCl with and without angiotensin and determining specific activity of Na ion with time. 2. Changes in CSF (Na ion) in rabbits (via an ion electrode) in normal and dehydrated states and correlation with p (Na ion), pADH, PRA and water consumption. 3. Evaluation (anesthetized rats) of whether central or peripheral infusions of high or low (NA ion) alters CSF angiotensin and ADH efflux. All known biological effects of angiotensin require sodium. Central nervous angiotensin administration increases blood pressure and causes natriuresis. The proposed studies should determine if the mechanism of angiotensin is altered movement of sodium between blood and brain.